|Volume 5||Summer 2001|
"Genetic Influences on Human Behavior and Development"
Genetic Influences on Human Behavior and Development
Responses to a question posed to presenters
and participants at the
A: Current advances in genetic research suggest that the old dichotomy between "genes" and "environment" is dead. "Genes" and "environment" don't act as independent influences on development. Many environmental influences initiate changes in gene expression. For example, in rats, effective maternal care changes the expression of genes in the brain that respond to stress hormones. Likewise, many genes require changes in the social environment in order to exert their influence. Human and animal studies suggest that effective parental care may thwart the expression of adverse genes on aggressive behavior in youngsters.
A: The era-or, perhaps, better, error-of genetic reductionism is over. The conference made clear that genes do not constrain human development but, rather, as parts of a dynamic, developmental system, are plastic entities that both influence and are influenced by the other levels or organization (cells, tissues, organs, and the physical, social, and cultural ecology) within this system. Reductionist models of gene action-such as behavior genetics or sociobiology-are now understood as egregiously flawed, counterfactual approaches to gene activity. Developmental systems models provide both a scientifically useful approach to understanding gene activity and a sound basis for applications to social policies aimed at promoting positive human development.
A: While I am awed by the scientific progress made in mapping the human genome, I believe that much of the knowledge generated in this enterprise represents indeterminant and relatively weak forces in human development. Information about genes will no doubt influence the practice of medicine and psychiatry in the prevention and treatment of many disorders, but this information is likely to recede to the background as new interventions are developed. The foreground will be occupied by social, political, economic and behavioral factors that are increasing within the control of human organizations and which are more directly involved in determining well-being.
A: My premise is that human behavior can influence genetic inheritance. Restricted mate selection due to belief systems or ethnic conflict can produce or enhance genetic differences between groups of people living in the same geographic area.
As a physician-scientist and director of an HIV prevention program in a small rural town in Guatemala, I have become involved in behavior modification as an HIV prevention strategy. HIV is a lethal disease that is not only transmitted by particular types of sexual behavior, but also from mother to neonate.
One behavior all human beings share is the ability to discriminate "us" from "them." This behavior is necessary for kin selection, a well-documented evolutionary force. I propose a theory of non-kin rejection as a corollary to kin selection, and suggest that the ability to discriminate between family and others influences mate selection. Furthermore, flexibility programmed into the human genome can result in environmentally influenced behavior that in turn affects inheritance of genetically encoded behavioral traits. Understanding the cues that determine kin selection, non-kin rejection and mating choice could help us devise an intervention and prevention strategy to stem the spread of HIV. But we also need to examine very carefully what the long-range consequences of such intervention will be on culture and on inheritance.
A: We have asked how we can reconcile our vision of ourselves as conscious decision-makers with the undeniable role of genes in explaining the differences and perhaps the similarities among us. We have also considered what the practical implications of research might be of the impact of genes on behavior. We begin by noting that though genes influence behavior, this neither justifies the behavior, nor means that it is inevitable. Even very high heritability of a behavioral trait does not imply inevitability, as reciprocal influences between environment and phenotype can amplify either genetic or persistent environmental differences, as shown by Dickens and Flynn in their April 2001 article in Psychological Review. In fact, high heritability may be a signal that reciprocal influences are multiplied so that persistent environmental stresses can have very large effects on phenotype. We go on to explore several models for how genes might influence behaviors that are compatible with the notion that people are decision-makers and generally do not act purely on instinct. We argue that, for the most part, the fact that genes influence behavior has few practical implications. However, we do identify some ways in which behavioral genetics and evolutionary psychology could make practical contributions which might improve our lives. We suggest the possibility that evolutionary psychology might provide a rigorous foundation for the newly emerging field of behavioral economics leading to greater acceptance and application of work in that field.
A: Questions of the form "what is the proportion of genetic influence on a trait or behavior" ultimately have no meaning. They are based on reductionist, non-developmental models of the determinants of human behavior. Furthermore, the questions (and resulting answers) can be destructive from a humanistic and policy perspective. They confer errors in meaning as follows. First is the implication of individual locus for behaviors which, in fact, are embodied within person-in-context systems. Also, genetic attribution implies that individuals have diminished responsibility for their behavior - their behavior is determined by their biology. Second, genetic theories are often interpreted as explaining stable traits. Even though many behavior geneticists take great pains to emphasize that development is important, the basic model fundamentally requires estimates regarding an individual characteristic - why make such estimates about characteristics that are unstable? Third, if one's biology emanating from DNA explains behavioral variation, then altering that biology is a logical way of altering behavior. Pharmacologic agents are a common method for altering biology, but we see all too often in the treatment of behavior disorders how simple medical interventions are used in place of contextualized analyses of behavior because they are cheaper and easier to implement and manage. Two poor outcomes result - less than optimal intervention for problematic behavior combined with unintended side effects of medical therapy.
A: The heritability concept must be distinguished from the heredity concept because social policy based on inappropriate heritability statistics risks misguided predictions about child development in present and future society. Heredity is our name for the biological system that makes possible the existence and reproduction of each species, while heritability was developed in the mid 1930's to predict the outcome of plant and animal breeding studies. It was borrowed by some psychologists in the belief that it could be applied to human data, in works like The Bell Curve, to determine what proportion of IQ is inherited (nature) and how much is acquired through experience (nurture). Usually the heritability statistic measures the additive genetic variance of a trait in a population and may be quite different in one population from that in another population of one species. However analysis of the limitations of heritability reveals its inappropriateness as a measure in human psychology (Hirsch, 1997; Kempthorne, 1978; Jacquard, 1983) where breeding experiments are off limits.
A: It is clear that we must attempt to understand how genes contribute to psychological development. Over time an individual's DNA sequence is invariant, but gene expression changes in response to the internal and external environments and these changes in gene expression are important in development. Genetic research is especially useful in addressing such questions as, why do children differ from one another at a single or across multiple ages, but it is currently less useful for questions of why people change on average between two ages. Although enthusiasm is high regarding the potential contributions of molecular biology to behavior genetics, multiple small effects, numerous interactions, complicated pathways, and chaotic complexity will always be the null hypothesis. In summary, optimism, humility, and perseverance are required for research in behavior genetics, as they are for most psychological inquiry.
A: Nature, nurture and developmental outcomes: Not "how much?" but rather "how?" (Spencer & Harpalani, 2001). Traditionally, the discipline of behavioral genetics focuses on measuring how much variance within populations can be attributed to genetic or environmental factors. For developmental psychologists, the pertinent question is not "how much?" but rather, "how?" (Bronfenbrenner & Ceci, 1994). By what mechanisms do heredity and environment interact to produce observable outcomes? To answer this question, issues of identity and context must be taken into account along with genetic factors. Spencer's (1995) Phenomenological Variant of Ecological Systems Theory (PVEST) provides a systems-focused, process-oriented developmental framework to analyze nature-nurture interaction. See cited references for more detail.
A: Two views of behavioral genetics (BG) were presented at the Brown University Genetics Conference. One view concerns quantitative or population behavior genetics and involves the heritability statistic (H2). Population behavior genetics is not applicable to the understanding of individual development, though it is often incorrectly used in that way. The calculation of H2 is based on the ANOVA statistic which partitions (divides) the variance of phenotypes proportionately into two supposedly independent components: a supposed independent genetic (G) component (not directly measured) and a supposed independent environmental (E) component (also not directly measured). In this approach, as an example, G could account for 60% of the variance and, therefore, E would account for the remaining 40% of the variance in a population. The ANOVA is relatively insensitive to interaction, so it often allows one to conclude there is no G-E interaction.
The other approach to BG is a developmental one, in which G-E interaction is the major concern. Interaction is present in the development of all phenotypes, not just some phenotypes. These two approaches are incommensurate, not complementary. Since genes are involved in all phenotypic outcomes, except in cases like fragile X mental retardation and other disorders, in which the problem is a lack of gene expression, the quantitative behavior genetic approach provides no information (or misleading information) as far as individual development is concerned. In discussing the lack of 100% concordance for schizophrenia in identical twins, for example, someone told me that was due to "incomplete penetrance". Incomplete penetrance is a population concept, which means that a gene has not yet spread to all members in a population. It does not apply to individual development as if gene expression was lacking in an individual.
As Professors Robert Plomin, Michael Rutter, and other BG'ers now believe, behavior geneticists need to focus on identifying the actual genes that are correlated with any and all phenotypic outcomes, with the clinical exceptions mentioned above. The tools to do that are now available as specified in the presentation at the Brown University Conference given by Michael Pogue-Geile, a clinical psychologist from the University of Pittsburgh.
As I demonstrated in my talk, in order for genes to be activated they require signals from the internal and external environment. There is no autonomous or self-contained genetic program for human (or other animal) development. When identical twins reared apart are both found to whistle in elevators it is not just because they share the same genes. Genes in and of themselves do not make people whistle in elevators (or make people do anything at all). That is why the concordance for schizophrenia in identical twins is 28% instead of 100%. Identical twins reared together do not share all the pertinent experiences to develop schizophrenia, and these experiences can begin as early as in the early prenatal period in which they may or may not share the same placenta. Identical twins that share one placenta are more alike psychologically than ones that had their own placenta, (Phelps, J.A., et al., 1997) so that pertinent experiences begin in the prenatal period. A finding usually ignored or overlooked in studies of psychological development.
Even though this state of the art research is widely available, recent highly visible work (i.e. Herrstein and Murray, The Bell Curve, 1994; Harris, The Nurture Assumption, 1998; Rowe, The Limits of Family Influence, 1994 and Rushton, Race, Evolution and Behavior, 1995) continues to portray a distorted view of the role of genetics in human behavior and development with erroneous implications for public policy. The purpose of sharing the present information is to elucidate the complexity of these issues based on recent findings in a myriad of disciplines. As is clear from the brief descriptions of them, the contributors to this issue are distinguished scholars from developmental and comparative psychology, molecular biology, psychiatry, economics and ethics. They use their research to advocate for an inclusive yet highly dynamic view of the interplay between nature and nurture. Traditional questions of how much variance is attributed to biology or to the environment, or the preponderance of one versus the other, are seen as limited or irrelevant to our current endeavors. This information represents a timely contribution to a highly visible and controversial area with very important policy implications.